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Using shRNA to silence CD36 in LNCaP prostate cancer cells, the researchers found that treatment with SIM1-Me (10 nM) or ARV-110 (50 nM) led to: 5.6-fold and 19.6-fold reductions, respectively, in cellular drug uptake dramatically impaired target protein degradation markedly reduced cytotoxicity (up to 423-fold) Re-expression of CD36 restored activity, and loss of EEA1 also diminished SIM1-Me and ARV-110 cytotoxicity---confirming a dependence on the Rab5/EEA1 endocytic pathway

Research-Referenced Functional Attributes (Based on existing preclinical and literature datanot intended as claims of therapeutic use) High-affinity binding to HGF and potentiation of c-Met activation in the presence of subthreshold HGF concentrations in cellular assays (DOI: 10.1124/jpet.114.218735) Induction of synaptogenesis and dendritic spine formation through HGF/c-Met pathway augmentation in neuronal models Observation of PI3K/AKT signaling modulation in APP/PS1 mouse models (DOI: 10.3389/fnagi.2021.748253) Investigation of neuroregenerative signaling mechanisms in scopolamine-induced impairment paradigms Examination of synaptic protein expression markers in aging or stress-challenged experimental systems Examination of oral bioavailability and blood-brain barrier penetration in rodent studies